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linolenic acid/emlőrák
A hivatkozás a vágólapra kerül
Oldal 1 tól től 114 eredmények
Concentration-dependent effect of iron on gamma-linolenic acid toxicity in ZR-75-1 human breast tumor cells in culture.
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Polyunsaturated fatty acids are cytotoxic to ZR-75-1 human breast tumor cells in culture. This effect may be potentiated by the simultaneous addition of iron. When cytotoxicity was measured in the presence of different concentrations of both gamma-linolenic acid and ferrous chloride there was an
Peroxisome proliferator activated receptor-gamma (PPAR-gamma) mediates the action of gamma linolenic acid in breast cancer cells.
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Gamma linolenic acid (GLA) is a polyunsaturated fatty acid, which induces cytotoxicity and regulates cell adhesion in cancer cells. The molecular mechanism of these actions is not clear. We have shown that GLA acts via peroxisome proliferator activated receptors (PPARs), by stimulating their
Intracellular free Fatty-Acid release and lipid-peroxidation in cultured human breast-cancer cells in response to gamma-linolenic Acid with iron (gla + fe).
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Intracellular free fatty acid (FFA) release and peroxidation of polyunsaturated fatty acid (PUFA) were studied in cultured human breast cancer cells (ZR-75-1) exposed to gamma-linolenic acid with iron (GLA + Fe). This treatment results in cell death. Increased intracellular FFA were observed in
Effects of linoleic acid and gamma-linolenic acid on the growth and metastasis of a human breast cancer cell line in nude mice and on its growth and invasive capacity in vitro.
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It has been reported that gamma-linolenic acid (GLA)-rich diets suppress mammary carcinogenesis and transplanted tumor growth and that GLA inhibits the growth of cultured human cancer cell lines. We compared the effects of dietary GLA and linoleic acid (LA) on the growth of MDA-MB-435 human breast
α-linolenic acid and docosahexaenoic acid, alone and combined with trastuzumab, reduce HER2-overexpressing breast cancer cell growth but differentially regulate HER2 signaling pathways.
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BACKGROUND
Diets rich in the n-3 fatty acid alpha-linolenic acid (ALA) have been shown to reduce breast tumor growth, enhance the effectiveness of the HER2-targeted drug trastuzumab (TRAS) and reduce HER2 signaling in mouse models. It is unclear whether this is due to direct effects of ALA or due to
Comparison of stearidonic acid and alpha-linolenic acid on PGE2 production and COX-2 protein levels in MDA-MB-231 breast cancer cell cultures.
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The bioactivity of stearidonic acid (SDA, 18:4n-3) and alpha-linolenic acid (LNA, 18:3n-3) on cyclooxygenase-2 (COX-2) enzyme expression and prostaglandin E2 (PGE2) production has not been evaluated. This investigation examined the effects of SDA and LNA on PGE2 biosynthesis and COX-2 protein and
Low alpha-linolenic acid content of adipose breast tissue is associated with an increased risk of breast cancer.
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Data derived from experimental studies suggest that alpha-linolenic acid may have a protective effect in breast cancer. Observations obtained from epidemiological studies have not allowed conclusions to be drawn about a potential protective effect of dietary alpha-linolenic acid on breast cancer,
Lipid peroxidation in human breast cancer cells in response to gamma-linolenic acid and iron.
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Lipid peroxidation in human breast cancer (ZR-75-1) cells and cancer cell killing were confirmed by using ultraviolet (UV)-spectrophotometry and mass spectrometry (MS). ZR-75-1 cells and human normal fibroblast CCD-41-SK (41Sk) cells were cultured with gamma-linolenic acid (GLA) and ferrous iron Fe
alpha-Linolenic acid content of adipose breast tissue: a host determinant of the risk of early metastasis in breast cancer.
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The association between the levels of various fatty acids in adipose breast tissue and the emergence of visceral metastases was prospectively studied in a cohort of 121 patients with an initially localised breast cancer. Adipose breast tissue was obtained at the time of initial surgery, and its
Low eicosapentaenoic acid and gamma-linolenic acid levels in breast adipose tissue are associated with inflammatory breast cancer.
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Effect of gamma-linolenic acid on cellular uptake of structurally related anthracyclines in human drug sensitive and multidrug resistant bladder and breast cancer cell lines.
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This study investigated the effect on drug uptake in multidrug resistant cells by the incorporation of the essential fatty acid gamma-linolenic acid (GLA). The cell lines used were the MCF-7/R resistant human breast cancer and MGH-U1/R bladder cancer. Uptake of drug (doxorubicin, epirubicin,
HER2 (erbB-2)-targeted effects of the omega-3 polyunsaturated fatty acid, alpha-linolenic acid (ALA; 18:3n-3), in breast cancer cells: the "fat features" of the "Mediterranean diet" as an "anti-HER2 cocktail".
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BACKGROUND
Data derived from epidemiological and experimental studies suggest that alphalinolenic acid (ALA; 18:3n-3), the main omega-3 polyunsaturated fatty acid (PUFA) present in the Western diet, may have protective effects in breast cancer risk and metastatic progression. A recent pilot clinical
α-Linolenic Acid Reduces Growth of Both Triple Negative and Luminal Breast Cancer Cells in High and Low Estrogen Environments.
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Flaxseed, rich in α-linolenic acid (ALA), is a complementary breast cancer (BC) therapy; however ALA effectiveness and mechanism are unclear. Variation in cellular expression of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and estrogen (E2)
Synergistic interaction between vinorelbine and gamma-linolenic acid in breast cancer cells.
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It has been suggested that exogenous unsaturated fatty acids (UFAs) may increase the cytotoxic activity of cancer chemotherapeutic agents. We examined how y-linolenic acid (GLA; 18: 3n-6), the most promising UFA in the treatment of human tumors, affects the effectiveness of the lipophilic drug
Gamma linolenic acid with tamoxifen as primary therapy in breast cancer.
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Gamma linolenic acid (GLA) has been proposed as a valuable new cancer therapy having selective anti-tumour properties with negligible systemic toxicity. Proposed mechanisms of action include modulation of steroid hormone receptors. We have investigated the effects of GLA with primary hormone therapy
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